AH metabolites/zinc chelators associated with POAG identified by GC-MS-based metabolomic analysis
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ABSTRACT:
INSTRUMENT(S): GCMS-QP2020
ORGANISM(S): Human
SUBMITTER: 
Dmitry Chistyakov
PROVIDER: MSV000093951 | MassIVE | Tue Jan 30 01:04:00 GMT 2024
REPOSITORIES: MassIVE
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Project description:AH metabolites/zinc chelators associated with POAG identified by GC-MS-based metabolomic analysis.
Methanol/chloroform extraction, derivatization - methoxylamine hydrochloride and of N,O-Bis(trimethylsilyl)trifluoroacetamide
2024-01-30 | MSV000093951 | GNPS
Project description:Steroids play a broad and vital role in regulation of gene expression, secondary sexual characteristics, maturation, reproduction, and neurological functions; but an imbalance in steroid metabolism is also linked to development and progression of many diseases including autism. Prenatal stress of different nature has been demonstrated to affect both the mother and the offspring. Adverse nutritional conditions during gestation can impair the maternal hypothalamic-pituitary-adrenal axis (HPA) and expose the fetus to high levels of glucocorticoids (GC). Evenwhen GC are required for normal brain development; an increased exposure of the fetus to GC as a consequence of prenatal stress can affect fetal hypothalamic-pituitary-gonad axis (HPG) development, impair neurogenesis, and have a long term impact on the offsprings mental health. Decreased zinc availability can occur during pregnancy as a consequence of different conditions (nutritional deficiency, infections, diabetes, alcohol consumption, and exposure to certain toxicants). Importantly, several of these gestational conditions have been linked to autism. In fact, alterations in maternal zinc homeostasis upon exposure to select environmental stressors (e.g. the phthalate plasticizer bis-2-ethylhexyl phthalate (DEHP)) that have become increasingly common since the industrial revolution may underlie the recent rise in the incidence of autism.Alterations in maternal zinc homeostasis could expose the fetus to high GC concentrations secondary to a high maternal GC production and/or to a decreased capacity of the placenta to metabolize GC to inactive metabolites. The overall goal of this proposal is to investigate if alterations in zinc homeostasis during gestation triggered by either a marginal zinc nutrition or exposure to an environmental pollutant (the phthalate plasticizer bis-2-ethylhexyl phthalate (DEHP)) can impair maternal and fetal endocrine signaling leading to impaired fetal brain development.
2014-09-30 | ST000120 | MetabolomicsWorkbench
Project description:Phase II randomized trial to investigate whether supplementation of zinc decreases the incidence of HFSR that occurs after treatment of tyrosine kinase inhibitor, regorafenib.
| 2301575 | ecrin-mdr-crc
Project description:Transcriptomics of Zinc-limited and Zinc-replete Mycobacterium tuberculosis
| PRJNA707587 | ENA
Project description:How cells safeguard essential zinc-dependent functions during zinc deficiency is poorly understood. A long-debated strategy is whether soluble metal-trafficking chaperones exist to prioritize specific zinc-dependent proteins. We identified a eukaryotic family of metallochaperones that physically interacts with zinc-dependent methionine aminopeptidase type I (MAP1) in human and yeast. Deletion of the yeast metallochaperone-encoding gene NMC1 (formerly YNR029c) leads to a zinc-deficiency growth defect and defective initiator methionine cleavage caused by loss of Map1p activity. To better understand the observed fitness defects due to the lack of NMC1 under zinc deficiency, we used proteomics with Tandem Mass Tag (TMT) quantitation derived from WT, nmc1Delta, and map2Delta nmc1Delta strains grown in zinc-limited (1 uM) or zinc-replete (100 uM) conditions. Proteomics reveal global impacts due to the loss of NMC1 and Map1p function, including mis-regulation of the Zap1p regulon, and suggests that Nmc1p is required to avoid a compounding effect of Map1p dysfunction on cell survival during zinc deficiency.
| MSV000088135 | MassIVE
Project description:This a model from the article:
The dynamic balance of import and export of zinc in Escherichia coli suggests a heterogeneous population response to stress
Takahashi H, Oshima T, Doherty N, Clayton SR, Iqbal M, Hill PJ, Hobman JL, Tobe T, Ogasawara N, Kanaya S and Stekel DJ
journal year
id,
Abstract:
Zinc is essential for life, but toxic in excess. Thus all cells must control their internal zinc concentration. We used a systems approach, alternating rounds of experiments and models, to further elucidate the zinc control systems in Escherichia coli. We measured the response to zinc of the main specific zinc import and export systems in the wild type, and a series of deletion mutant strains. We interpreted these data with a detailed mathematical model and Bayesian model fitting routines. There are three key findings: First, that alternate, non-inducible importers and exporters are important. Second, that an internal zinc reservoir is essential for maintaining the internal zinc concentration. Third, our data fitting led us to propose that the cells mount a heterogeneous response to zinc: some respond effectively, while others die or stop growing. In a further round of experiments we demonstrated lower viable cell counts in the mutant strain tested exposed to excess zinc, consistent with this hypothesis. A stochastic model simulation demonstrated considerable fluctuations in the cellular levels of the ZntA exporter protein, reinforcing this proposal. We hypothesise that maintaining population heterogeneity could be a bet-hedging response allowing a population of cells to survive in varied and fluctuating environments.
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
For more information see the terms of use.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2016-02-10 | MODEL1502180000 | BioModels
Project description:We evaluated the intestinal responses of pigs under zinc restriction and under different zinc sources through RNA-seq of ileal samples. We identified changes in genes related to zinc transport, immune response, cell proliferation, DNA damage and stress resposne. Our findings demonstrate that swine intestine is responsive to zinc restriction and can be a model sentinel tissue for human zinc deficiency. Further research is needed to define the intestinal responses to organic and inorganic zinc sources.
2021-08-05 | GSE181343 | GEO
Project description:This study addresses the impact of zinc limitation on the opportunistic human pathogen, Pseudomonas aeruginosa. Zinc limitation was assessed in the P. aeruginosa PAO1 strain using an isogenic deletion mutant lacking the periplasmic, zinc solute-binding protein, znuA (PA5498). ZnuA delivers bound zinc to its cognate ABC transporter, ZnuBC, for import into the cytoplasm. Our transcriptional analyses revealed P. aeruginosa to possess a multitude of zinc acquisition mechanisms, each of which were highly up-regulated in the zinc-deficient znuA mutant strain. P. aeruginosa also utilized zinc-independent paralogues of zinc-dependent genes to maintain cellular function under zinc limitation. Together, these data reveal the complex transcriptional response and versatility of P. aeruginosa to zinc depletion.
2017-01-01 | GSE60177 | GEO